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DOI: 10.1055/a-0646-7871
Das diabetische Herz und Herzinsuffizienz – Aktuelles zu Entstehung und Therapie
The Diabetic Heart and Heart Failure – Update on Mechanisms and TherapyPublikationsverlauf
Publikationsdatum:
31. Januar 2019 (online)
![](https://www.thieme-connect.de/media/dmw/201903/lookinside/thumbnails/dmw-6467871_10-1055-a-0646-7871-1.jpg)
Was ist neu?
Klinisches Bild Typ-2-Diabetes-mellitus (T2 D) ist ein unabhängiger Risikofaktor für Herzinsuffizienz, die als Komplikation oftmals unterschätzt wird. Bei T2 D kann sich früh eine diastolische Funktionsstörung ausbilden, die sich später zu einer Herzinsuffizienz entwickeln kann. Von einer ischämischen Kardiomyopathie ist eine Diabetes-bedingte Herzinsuffizienz aktuell nicht abgrenzbar.
Pathophysiologie Hyperglykämie, Hyperinsulinämie und Hyperlipidämie bei T2 D verändern den myokardialen Stoffwechsel. Daraus resultieren oxidativer Stress, reduzierte mitochondriale Effizienz, Lipotoxizität und Apoptose im Herzen. Die T2D-assoziierte nicht-alkoholische Fettlebererkrankung (NAFLD) zeigt ähnliche Pathomechanismen und stellt einen potenziellen Risikofaktor dar.
Therapiestrategien Zur Verbesserung der Herzfunktion wird die Kontrolle kardiovaskulärer Risikofaktoren sowie Reduktion der Insulinresistenz durch Bewegung und Gewichtsabnahme empfohlen. Neben Metformin scheinen SGLT2-Inhibitoren als zusätzliche Therapieoption besonders geeignet zu sein. Auch die NAFLD könnte ein Angriffspunkt zukünftiger Therapieansätze werden.
Abstract
Type 2 Diabetes mellitus (T2 D) is an independent risk factor for cardiovascular diseases and non-ischemic heart failure, an underestimated complication of T2 D. Diastolic dysfunction is an early sign of diabetes-related heart failure preceding its progression to systolic damage. The etiology of heart failure in these patients has recently been partially unveiled. Along with other mechanisms, hyperinsulinemia and hyperlipidemia cause increased myocardial lipid accumulation and oxidation, which leads to lipotoxicity, oxidative stress, inflammatory response and eventually impaired mitochondrial efficiency, fibrosis, apoptosis and contractile dysfunction. These myocardial alterations resemble the cellular mechanisms underlying the development of non-alcoholic fatty liver disease (NAFLD), a frequent comorbidity of T2 D and another risk factor for cardiovascular diseases and heart failure. Control of risk factors, lifestyle intervention and antihyperglycemic treatment are the recommended treatment for patients with T2 D and heart failure. While thiazolidindiones and some dipeptidyl peptidase 4 (DPP4) inhibitors may be detrimental for patients with heart failure, recent studies provided evidence for safe use of glucagon-like peptide 1 (GLP1) receptor agonists and for possible beneficial effects of sodium glucose co-transporter 2 (SGLT2) inhibitors on mortality and hospitalization of T2 D patients with heart failure. Treatment of NAFLD could also be beneficial for the cardiovascular outcome of patients with T2D-related heart failure. This article provides a brief summary of the current research on underlying mechanisms, clinical features and recently recommended therapeutic approaches for T2D-related heart failure.
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